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      The Association of C-Reactive Protein with Subclinical Cardiovascular Disease in HIV-infected and HIV-uninfected Women

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          Abstract

          Objective

          HIV is a cardiovascular disease (CVD) risk factor. However, CVD risk is often underestimated in HIV-infected women. C-reactive protein (CRP) may improve CVD prediction in this population. We examined the association of baseline plasma CRP with subclinical CVD in women with and without HIV.

          Design

          Retrospective cohort study

          Methods

          572 HIV-infected and 211 HIV-uninfected women enrolled in the Women’s Interagency HIV Study underwent serial high-resolution B-mode carotid artery ultrasonography between 2004-2013 to assess carotid intima-media thickness (CIMT) and focal carotid artery plaques. We used multivariable linear and logistic regression models to assess the association of baseline high (≥3 mg/l) high-sensitivity (hs) CRP with baseline CIMT and focal plaques, and used multivariable linear and Poisson regression models for the associations of high hsCRP with CIMT change and focal plaque progression. We stratified our analyses by HIV status.

          Results

          Median (IQR) hsCRP was 2.2 mg/l(0.8-5.3) in HIV-infected, and 3.2 mg/l(0.9-7.7) in HIV-uninfected, women (p=0.005). There was no statistically significant association of hsCRP with baseline CIMT [adjusted mean difference -3.5 μm (95%CI:-19.0-12.1)] or focal plaques [aOR:1.31(0.67-2.67)], and no statistically significant association of hsCRP with CIMT change [adjusted mean difference 11.4 μm(-2.3-25.1). However, hsCRP ≥3 mg/l was positively associated with focal plaque progression in HIV-uninfected [aRR:5.97(1.46-24.43)], but not in HIV-infected [aRR:0.81(0.47-1.42)] women (p=0.042 for interaction).

          Conclusion

          In our cohort of women with similar CVD risk factors, higher baseline hsCRP is positively associated with carotid plaque progression in HIV-uninfected, but not HIV-infected, women, suggesting that subclinical CVD pathogenesis may be different HIV-infected women.

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          Author and article information

          Journal
          8710219
          1493
          AIDS
          AIDS
          AIDS (London, England)
          0269-9370
          1473-5571
          14 March 2018
          15 May 2018
          15 May 2019
          : 32
          : 8
          : 999-1006
          Affiliations
          [1 ]Department of Medicine, Emory University, Atlanta, GA 30322, USA
          [2 ]Grady Healthcare System, Atlanta, GA 30303, USA
          [3 ]Department of Biostatistics and Bioinformatics, Emory University, Atlanta, GA 30322, USA
          [4 ]Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA
          [5 ]Department of Neurology, State University of New York- Downstate, Brooklyn, NY 11203, USA
          [6 ]Department of Medicine, Georgetown University Medical Center, Washington, DC 20007, USA
          [7 ]Department of Preventive Medicine, University of Southern California, Los Angeles, CA 90033, USA
          [8 ]Department of Medicine, University of Southern California- San Francisco and the Department of Veterans Affairs, San Francisco, CA 94121, USA
          [9 ]Department of Medicine, Stroger Hospital of Cook County and Rush University Medical Center, Chicago, IL 60612, USA
          [10 ]Department of Epidemiology, Johns Hopkins University, Baltimore, MD 21205, USA
          Author notes
          Address correspondence and requests for reprints to: Caitlin Moran, Division of Infectious Diseases, Emory University School of Medicine, 49 Jesse Hill Jr Drive, Atlanta, GA 30303; Tel: (404) 778-1620; Fax: (404) 616-0592; cmoran4@ 123456emory.edu
          Article
          PMC5920777 PMC5920777 5920777 nihpa950484
          10.1097/QAD.0000000000001785
          5920777
          29438198
          7e56b2c5-d87a-4be0-9916-960e288ce280
          History
          Categories
          Article

          atherosclerosis,subclinical CVD,women,HIV,C-reactive protein

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